Abnormal sensory experiences, including chronic pain, frequently develop following spinal cord injury (SCI). We hypothesize that one potential source of such abnormal sensations could be neurons rostral to the lesion that have, as a result of SCI, lost their normal tonic modulation from propriospinal and/or descending control systems. The plasticity of spinal dorsal horn neuronal responses to receptive field stimulation is now well established. Pilot work in our laboratory, using an awake, drug-free animal preparation to study sensory processing in single spinal dorsal horn neurons (a unique aspect of this proposed study) has revealed that damage to the spinal cord increases the likelihood that some neurons will respond to stimuli approaching or within the noxious range. We have shown that a similar increase in response to noxious stimuli can be produced by the pharmacologic blockade of known inhibitory systems (i.e., loss of tonic modulation, unmasking of neuronal plasticity). By recording extracellularly from single spinal lumbar dorsal horn neurons above selective lesions in awake, drug-free cats we propose to answer the following questions: 1) What is the likelihood that a gross caudal lesion in the spinal grey will increase the number of spinal dorsal horn neurons responding to a noxious stimulus? 2) Will more discrete lesions directed at propriospinal or descending modulatory systems produce similar changes in the probability of increased response to noxious stimulation time- dependent within three months following the lesion? Using behavioral tests, we propose to correlate observed changes in neurophysiology with changes in animal response to non-noxious and mildly noxious mechanical and thermal skin stimulation. Finally, we will use and receptor autoradiography to examine changes in transmitter systems that could account for any observed increase in response to noxious stimulation. Information about changes in sensory processing and the transmitter systems that may contribute to those changes may lead to unique ways to pharmacologically reverse abnormal sensory experiences that occur following SCI.